CHAPTER 33 THERAPY OF ASTHMA, CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) AND OTHER RESPIRATORY DISORDERS ● Pathophysiology of asthma 233 ● Management of acute severe asthma 233 ● Chronic asthma 234 ● Acute bronchitis 235 ● Chronic bronchitis and emphysema 235 ● Drugs used to treat asthma and chronic obstructive pulmonary disease 236 PATHOPHYSIOLOGY OF ASTHMA Asthma is characterized by fluctuating airways obstruction, with diurnal variation and nocturnal exacerbations. This manifests as the triad of wheeze, cough and breathlessness. These symptoms are due to a combination of constriction of bronchial smooth muscle, oedema of the mucosa lining the small bronchi, and plugging of the bronchial lumen with viscous mucus and inflammatory cells (Figure 33.1). Asthma is broadly categorized into non-allergic and allergic, but there is considerable overlap. In allergic asthma, which is usually of early onset, extrinsic allergens produce a type I allergic reaction in atopic subjects. Type I reactions are triggered via reaginic antibodies (IgE) on the surface of mast cells and other immune effector cells, especially activated Th2 lymphocytes, which release cytokines that recruit eosinophils and promote further IgE synthesis and sensitivity. Patients with non-allergic (late-onset) asthma do not appear to be sensitive to any single well-defined antigen, although infection (usually viral) often precipitates an attack. Inflammatory mediators implicated in asthma include histamine, several leukotrienes (LTC 4/D 4 and E 4) 5-hydroxytryptamine (serotonin), prostaglandin D 2, platelet-activating factor (PAF), neuropeptides and tachykinins. Increased parasympathetic tone due to local and centrally mediated stimuli also promotes bronchoconstriction. ● Respiratory failure 241 ● Cough 242 ● α 1-Antitrypsin deficiency 242 ● Drug-induced pulmonary disease 243 MANAGEMENT OF ACUTE SEVERE ASTHMA The proposed management is based on the British Thoracic Society guidelines and involves the following: • assessment of asthma severity (e.g. unable to complete sentences in one breath, pulse rate and pulsus paradox, if measurable, respiratory rate, breath sounds peak expiratory flow rate, pulse oximetry and blood gases if arterial O 2 saturation �92%) to define the need for hospitalization. Life-threatening asthma (e.g. silent chest, exhaustion, cyanosis, peak flow �33% of predicted or best, saturation �92%) needs urgent treatment with: • high flow oxygen (FiO 2 40–60% oxygen); • glucocorticosteroids: hydrocortisone i.v., followed by prednisolone p.o.; • nebulized β 2-agonist (e.g. salbutamol) plus ipratropium; via oxygen-driven nebulizer; • if the response to the above bronchodilator treatment is inadequate or not sustained, consider intravenous bronchodilator: β 2-agonist (e.g. salbutamol by i.v. infusion), or aminophylline/theophylline (by slow i.v. injection); • in refractory cases, consider magnesium sulphate (slow i.v. injection/short infusion);
234 THERAPY OF ASTHMA, COPD AND OTHER RESPIRATORY DISORDERS Omalizumab Cromoglicate Nedocromil �ve IgE IgE Allergic stimulus IgE • an antibiotic (e.g. co-amoxiclav or clarithromycin), if bacterial infection is strongly suspected – beware potential interactions with theophylline, see below; • if the patient fails to respond and develops increasing tachycardia, with increasing respiratory rate and a fall in PaO 2 to �8 kPa or a rise in PaCO 2 to �6 kPa, assisted ventilation will probably be needed; • sedation is absolutely contraindicated, except with assisted ventilation. • general care: monitor fluid/electrolyte status (especially hypokalaemia) and correct if necessary. CHRONIC ASTHMA IgE �ve Mediator cell IgE T� cell Leukotriene modulators Interleukin-4 �ve Interleukin-5 �ve IgE production IgE �ve B� cell �ve �ve The primary objectives of the pharmacological management of chronic asthma are to obtain full symptom control, prevent exacerbations and achieve the best possible pulmonary function, with minimal side effects. The British Thoracic Society/Scottish Intercollegiate Guideline Network (BTS/SIGN) have proposed a five-step management plan, with initiation of therapy based on the assessed severity of the disease at that timepoint. Figure 33.2 details the treatment in the recommended steps in adult asthmatics. Step 1 is for mild asthmatics with intermittent symptoms occurring only once or twice a week; step 2 is for patients with more symptoms (more than three episodes of asthma symptoms per week or nocturnal symptoms). Step 3 is for patients who have continuing symptoms despite step 2 treatment and steps 4 and 5 are for more chronically symptomatic patients or patients with worsening symptoms, despite step 3 or 4 treatment. � 2 -Agonists Antimuscarinics Theophylline Smooth muscle contraction �ve Histamine, LT, PGs, PAF, adenosine Eosino– phil �ve PAF, LTS Basic proteins �ve Glucocorticosteroids �ve �ve Bronchial smooth muscle Inflammatory mucus plug PRINCIPLES OF DRUG USE IN TREATING CHRONIC ASTHMA Inhibitory effects Stimulatory effects Episodic wheeze Chronic symptoms Wheeze Bronchial hyper-responsiveness Figure 33.1: Pathophysiology of asthma and sites of drug action. PAF, platelet-activating factor; LTs, leukotrienes; PGs, prostaglandins. 1. Metered dose inhalers (MDIs) of β 2-agonists are convenient and with correct usage little drug enters the systemic circulation. Aerosols are particularly useful for treating an acute episode of breathlessness. Long-acting β 2-agonist (e.g. salmeterol) should be taken regularly with top-ups of ‘on-demand’ shorter-acting agents. Oral preparations have a role in young children who cannot co-ordinate inhalation with activation of a metered-dose inhaler. Children over five years can use inhaled drugs with a ‘spacer’ device. There are several alternative approaches, including breath-activated devices and devices that administer the dose in the form of a dry powder that is sucked into the airways. 2. Patients should contact their physician promptly if their clinical state deteriorates or their β 2-agonist use is increasing. 3. Inhaled glucocorticosteroids (e.g. beclometasone, fluticasone, budesonide) are initiated when symptoms are not controlled or when: • regular (rather than occasional, as needed) doses of short-acting β 2-agonist bronchodilator are required; • repeated attacks interfere with work or school. Adverse effects are minimized by using the inhaled route. Severely affected patients require oral glucocorticosteroids (e.g. prednisolone).
Soliman s Auricular Therapy Textbook: New Localizations and Evidence Based Therapeutic Approaches was created ( M.D. Nader Soliman )
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Soliman s Auricular Therapy Textbook This textbook is considered the finest ever written in the field of auricular therapy. The auricular acupuncture microsystem is one of the most widely used special acupuncture techniques. This textbook is dedicated to teaching the sound foundations of this unique approach as introduced by its founder Dr. Paul Nogier of France. The scientific bases of the acupuncture microsystem with its three dime... Full description
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